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Nature medicine, ISSN 1546-170X, 01/2016, Volume 22, Issue 2, pp. 175 - 182
.... In mice, RIP3 deficiency or CaMKII inhibition ameliorates myocardial necroptosis and heart failure induced by ischemia-reperfusion or by doxorubicin treatment... 
Biochemistry & Molecular Biology | Life Sciences & Biomedicine | Medicine, Research & Experimental | Science & Technology | Cell Biology | Research & Experimental Medicine | Immunohistochemistry | Myocardial Ischemia - genetics | Receptor-Interacting Protein Serine-Threonine Kinases - metabolism | Phosphorylation | Antibiotics, Antineoplastic - toxicity | Reactive Oxygen Species | Oxidative Stress | Apoptosis - genetics | Necrosis - pathology | Membrane Potential, Mitochondrial | Myocardial Reperfusion Injury - genetics | Real-Time Polymerase Chain Reaction | Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism | In Situ Nick-End Labeling | Mitochondrial Membrane Transport Proteins - metabolism | Cell Survival | Mice, Inbred C57BL | Rats | Heart Failure - genetics | Heart Failure - pathology | Rats, Sprague-Dawley | Blotting, Western | Doxorubicin - toxicity | Mice, Knockout | Myocardial Ischemia - pathology | Calcium-Calmodulin-Dependent Protein Kinase Type 2 - genetics | Microscopy, Confocal | Myocardial Reperfusion Injury - metabolism | Myocytes, Cardiac - pathology | Receptor-Interacting Protein Serine-Threonine Kinases - genetics | Animals | Myocardial Ischemia - complications | Necrosis - etiology | Myocytes, Cardiac - metabolism | Mice | Necrosis - genetics | Heart Failure - chemically induced | Oxidative stress | Medical research | Physiological aspects | Medicine, Experimental | Research | Heart diseases | Necrosis | Apoptosis | Signal transduction | Cardiovascular disease | Cardiomyocytes | Ischemia | Index Medicus
Journal Article
Journal Article
The New England journal of medicine, ISSN 1533-4406, 04/2012, Volume 366, Issue 15, pp. 1404 - 1413
...-induced platelet aggregation. 6 , 7 This study, called the Thrombin Receptor Antagonist in Secondary Prevention of Atherothrombotic Ischemic Events (TRA 2P... 
Medicine, General & Internal | Life Sciences & Biomedicine | General & Internal Medicine | Science & Technology | Cardiovascular Diseases - prevention & control | Humans | Middle Aged | Male | Risk | Secondary Prevention | Pyridines - adverse effects | Cardiovascular Diseases - mortality | Female | Platelet Aggregation Inhibitors - therapeutic use | Platelet Aggregation Inhibitors - adverse effects | Pyridines - therapeutic use | Double-Blind Method | Hemorrhage - epidemiology | Receptor, PAR-1 - antagonists & inhibitors | Kaplan-Meier Estimate | Peripheral Arterial Disease - drug therapy | Stroke - drug therapy | Lactones - adverse effects | Lactones - therapeutic use | Retreatment | Myocardial Infarction - drug therapy | Brain Ischemia - drug therapy | Intracranial Hemorrhages - chemically induced | Intracranial Hemorrhages - epidemiology | Aged | Hemorrhage - chemically induced | Prevention | Drugs | Aggregation | Dose-response relationship (Biochemistry) | Atheroembolism | Blood platelets | Atherosclerosis | Product/Service Evaluations | Dosage and administration | Drug therapy | Myocardial infarction | Cerebral infarction | Stroke | Aspirin | Heart attacks | Proteinase-activated receptor 1 | Thrombin | Hemorrhage | Patients | Bleeding | Disease prevention | Ischemia | Arteriosclerosis | Death | Cardiovascular diseases | Health risk assessment | Index Medicus | Abridged Index Medicus | Computer Science | Medical Imaging
Journal Article
American journal of physiology. Heart and circulatory physiology, ISSN 0363-6135, 2015, Volume 308, Issue 9, pp. H998 - H1006
Increases in airborne particulate matter (PM) are linked to increased mortality from myocardial ischemia... 
Rat | Particulate matter | Pressure volume | Cardiac toxicity | Cardiac & Cardiovascular Systems | Physiology | Peripheral Vascular Disease | Life Sciences & Biomedicine | Cardiovascular System & Cardiology | Science & Technology | Myocardial Reperfusion Injury - etiology | Particulate Matter - toxicity | Myocardial Infarction - chemically induced | Myocardial Reperfusion Injury - chemically induced | Male | Ventricular Dysfunction, Left - chemically induced | Myocardial Reperfusion Injury - pathology | Time Factors | Inhalation Exposure | Myocardial Infarction - pathology | Myocardium - metabolism | Ventricular Dysfunction, Left - pathology | Myocardial Infarction - physiopathology | Myocardial Infarction - etiology | Disease Models, Animal | Free Radicals - toxicity | Risk Assessment | Risk Factors | Ventricular Function, Left - drug effects | Ventricular Pressure - drug effects | Stroke Volume - drug effects | Ventricular Dysfunction, Left - etiology | Myocardium - pathology | Myocardial Infarction - metabolism | Rats, Sprague-Dawley | Myocardial Reperfusion Injury - physiopathology | Ventricular Dysfunction, Left - physiopathology | Particle Size | Ventricular Dysfunction, Left - metabolism | Myocardial Reperfusion Injury - metabolism | Animals | Oxidative Stress - drug effects | Medical research | Ischemia | Medicine, Experimental | Research | Free radicals (Chemistry) | Health aspects | Reperfusion injury | Particles | Hydrocarbons | Free radicals | Airborne particulates | Mortality | Index Medicus | Call for Papers | particulate matter | cardiac toxicity | rat | pressure volume
Journal Article
Cardiovascular therapeutics, ISSN 1755-5914, 04/2015, Volume 33, Issue 2, pp. 27 - 34
.... In the present study, the effect of PPI pantoprazole on ventricular arrhythmias induced by either ischemia or ischemia–reperfusion (I/R) was studied... 
Ventricular arrhythmias | Proton pump inhibitors | Pantoprazole | Ischemia/reperfusion | Cardiac & Cardiovascular Systems | Pharmacology & Pharmacy | Life Sciences & Biomedicine | Cardiovascular System & Cardiology | Science & Technology | Proton Pump Inhibitors - pharmacology | Arrhythmias, Cardiac - chemically induced | Rats, Wistar | Myocardial Reperfusion Injury - complications | Anti-Arrhythmia Agents - pharmacology | Tachycardia, Ventricular - chemically induced | Male | 2-Pyridinylmethylsulfinylbenzimidazoles - pharmacology | Arrhythmias, Cardiac - physiopathology | Time Factors | Ventricular Premature Complexes - prevention & control | Ventricular Premature Complexes - physiopathology | Myocardial Ischemia - physiopathology | Ventricular Fibrillation - physiopathology | Myocardial Reperfusion Injury - blood | Disease Models, Animal | Ventricular Fibrillation - prevention & control | Arrhythmias, Cardiac - prevention & control | Nitric Oxide - blood | Anti-Arrhythmia Agents - toxicity | Myocardial Ischemia - blood | Heart Conduction System - drug effects | Tachycardia, Ventricular - prevention & control | Proton Pump Inhibitors - toxicity | Myocardial Reperfusion Injury - physiopathology | Ventricular Premature Complexes - chemically induced | 2-Pyridinylmethylsulfinylbenzimidazoles - toxicity | Tachycardia, Ventricular - physiopathology | Animals | Heart Conduction System - physiopathology | L-Lactate Dehydrogenase - blood | Myocardial Ischemia - complications | Ventricular Fibrillation - chemically induced | Hyperkalemia - chemically induced | Arrhythmias, Cardiac - blood | Arrhythmia | Ischemia | Nitric oxide | Mortality | Anti-arrhythmia drugs | Index Medicus
Journal Article
Journal Article
PloS one, ISSN 1932-6203, 2019, Volume 14, Issue 11, pp. e0225185 - e0225185
Journal Article